Impact of Traditional and E-Cigarette Smoking Metabolites on Acute Myeloid Leukemia
Abstract
Introduction:
Acute myeloid leukemia (AML) is a highly aggressive hematological malignancy with a notably poor prognosis. FMS-like tyrosine kinase 3 (FLT3) mutant AML is linked to a worse prognosis, which is found in 25% of AML cases among adolescents and young adults (AYA). Cigarette smoking leads to reduced survival rates in patients with AML. Tobacco products, including cigarettes, smokeless tobacco, and e-cigarettes contain nitrosamines like N′-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Many of these tobacco metabolites have been associated with oxidative stress and adaptive responses which may confer resistance to chemotherapy but have not been examined in the context of AML and smoking. Since AYA cancer patients are prone to unhealthy habits such as smoking and vaping, understanding the effects of nicotine metabolites on FLT3-mutant AML has potential to lead to better clinical management of patients who use or have used tobacco products.
This study investigates the effects of cigarette smoke condensate (CSC) and tobacco-specific nitrosamines (TSNAs) on FLT3-mutated AML cell lines and in vivo models to elucidate how smoking compounds influence AML progression and oxidative stress responses.
Methods:
FLT3-ITD-mutant AML cell lines (MOLM-13, MOLM-14) and non-FLT3 OCI-AML3 cells were treated with cigarette smoke condensate (CSC), NNN, and NNK, or vehicle controls for 2 weeks. Cell viability and proliferation were assessed using the…
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